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中国医科大学:《医学遗传学》课程教学资源(PPT课件)第九章 人类疾病的分子遗传学——血红蛋白病
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人类疾病的分子遗传学(PPT讲稿)血友病
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Neurodegenerative diseases and ubiquitin-proteasome syster to copyright considerations See Figure chanover, A and Brundin, P. 2003. The ubiquitin proteasome enerative diseases: sometimes the chicken, sometimes the egg
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《实验动物学》课程PPT教学课件(讲稿)第十章 人类疾病动物模型概述
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Reversible ligation of Ubiquitin and Ubls to other proteins. Figure by MIT OCW. After Figure 1 in Hochstrasser M. Evolution and function of ubiquitin-like protein-conjugation systems. Nat Cell Biol. 2000 Aug:
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Rip: REGULATED INTRAHENBRANE PROTEOLYSis .Site. spacifie membrae. prote2ses Substratey achivated by protcolytc procassing .. SREBP TF controlling rol metabohis IRE1 Unfolded protein response Notch APP \RoP*: REGULATED. UBiQUiTIN/PROTEASOME DEPENDENT PROCESSING\ type ERAD (ER zciakd dxgradatin) process involving proltoly'c procassing:
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正逆转录病毒亚科 (Orthoretrovirinae) Retroviridae 泡沫逆转录病毒亚科 (Spumavirinae) 未发现与人类疾病有关 慢病毒属 Lentivirus: 人免疫缺陷病 毒(HIV-1,2) 丁型逆转录病毒属 Deltaretrovirus:人 嗜T淋巴细胞病毒I型 (HTLV-1)
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How p53 and Rb pathway function may be disrupted in cancer cells Components of the pathway which are found altered in human cancers are shown in red on the diagram above p53 and Rb themselves may be inactivated by gene mutation (loss of both copies or also as in familial retinoblastoma and Li-Fraumeni syndrome where there are inherited mutations in one copy of Rb or p53 gene respectively. Alternatively
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insolubility. Administration of cystamine, a transglutaminase inhibitor, reduces the To date, 10 neurological diseases, including aggregate formation, retarding the Huntington's and several ataxias, are caused development of neurological phenotype and by the lengthening of glutamine(@) tracts in prolonging the life span of brain cells in various proteins with no obvious functional or transgenic mouse models
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Figure 2 in Muratani M, Tansey WP. \How the ubiquitin-proteasome system controls transcription.\ Nat Rev Mol Cell Biol. 2003 Mar; 4(3): 192-201. Regulation of TCR by ubiquitylation of RNA polymerase II. Transcription-coupled repair (TCR)is the mechanism through which mutations in actively transcribed genes are preferentially repaired. a Elongating RNA polymerase II (pol II)
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